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MicroRNA-150 enhances radiosensitivity by inhibiting the AKT pathway in NK/T cell lymphoma

BACKGROUND: Radioresistance is a major challenge during the treatment of NK/T cell lymphoma. This study aimed to investigate the potential role of MicroRNA-150 (miR-150) in increase the sensitivities of NK/T cell lymphoma to ionizing radiation. RESULTS: In this study, we found that miR-150 was signi...

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Detalles Bibliográficos
Autores principales: Wu, Shao Jie, Chen, Jun, Wu, BingYi, Wang, Yu Jue, Guo, Kun Yuan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5793389/
https://www.ncbi.nlm.nih.gov/pubmed/29386059
http://dx.doi.org/10.1186/s13046-017-0639-5
Descripción
Sumario:BACKGROUND: Radioresistance is a major challenge during the treatment of NK/T cell lymphoma. This study aimed to investigate the potential role of MicroRNA-150 (miR-150) in increase the sensitivities of NK/T cell lymphoma to ionizing radiation. RESULTS: In this study, we found that miR-150 was significantly decreased in NK/T cell lymphoma tissues and cell lines. Low expression of miR-150 was positively associated with therapeutic resistance in 36 NK/T cell lymphoma cases. Our further in vitro and in vivo studies illustrated that overexpression of miR-150 substantially enhanced the sensitivity of NK/T cell lymphoma cells to ionizing radiation treatment. Furthermore, luciferase reporter assays in NK/T cell lymphoma cells transfected with the AKT2 or AKT3 three prime untranslated region reporter constructs established AKT2 and AKT3 as direct targets of miR-150. The phosphatidylinositol 3-kinase inhibitor LY294002 was used to inhibit Akt to verify miR-150 increase NK/T cell lymphoma cell radiorsensitivity through suppress the PI3K/AKT/mTOR pathway. CONCLUSIONS: Taken together, this study demonstrates that miR-150 might serve as a potential therapeutic sensitizer through inhibition of the AKT pathway in NK/T cell lymphoma treatment. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s13046-017-0639-5) contains supplementary material, which is available to authorized users.